Pulmonary Hypertension Secondary to Heart Failure With Preserved Ejection Fraction

Thenappan, Thenappan; Prins, Kurt W.; Cogswell, Rebecca; Shah, Sanjiv J.

doi:10.1016/j.cjca.2014.12.028

Cited by 33 publications

(31 citation statements)

References 68 publications

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“…It has been demonstrated that chronic elevation in LV filling pressure leads to pulmonary venous congestion and post‐capillary pulmonary hypertension, regardless of LVEF . A reactive increase in pulmonary arterial tone or intrinsic arterial remodelling can result in a superimposed pre‐capillary component of pulmonary hypertension in more advanced stages, further aggravating the clinical situation . The development of pulmonary hypertension proved to be an excellent marker to distinguish HFpEF from HT in a large community‐based study, suggesting that it can play a key role in the transition .…”

Section: Discussionmentioning

confidence: 99%

“…[38][39][40][41][42] A reactive increase in pulmonary arterial tone or intrinsic arterial remodelling can result in a superimposed pre-capillary component of pulmonary hypertension in more advanced stages, further aggravating the clinical situation. 43 The development of pulmonary hypertension proved to be an excellent marker to distinguish HFpEF from HT in a large community-based study, suggesting that it can play a key role in the transition. 40 Also, pulmonary hypertension and its severity has a significant prognostic role, because it is associated with increased short-and long-term mortality both in HFpEF and HFrEF.…”

Section: Cardiovascular and Pulmonary Function During Exercisementioning

confidence: 99%

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Haemodynamic and metabolic phenotyping of hypertensive patients with and without heart failure by combining cardiopulmonary and echocardiographic stress test

Pugliese

Mazzola

Fabiani

et al. 2020

European J of Heart Fail

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Aim We combined cardiopulmonary exercise test (CPET) and exercise stress echocardiography (ESE) to identify early haemodynamic and metabolic alterations in patients with hypertension (HT) with and without heart failure with preserved ejection fraction (HFpEF). Methods and results Fifty stable HFpEF‐HT outpatients (mean age 68 ± 14 years) on optimal medical therapy, 63 well‐controlled HT subjects (mean age 63 ± 11 years) and 32 age and sex‐matched healthy controls (mean age 59 ± 15 years) underwent a symptom‐limited graded ramp bicycle CPET‐ESE. The acquisition protocol included left ventricular cardiac output, global longitudinal strain, E/e′, peak oxygen consumption (VO2), non‐invasive arterial–venous oxygen content difference (AVO2diff) and lung ultrasound B‐lines. There was a decline in peak VO2 from controls (24.4 ± 3 mL/min/kg) to HFpEF‐HT (15.2 ± 2 mL/min/kg), passing through HT (18.7 ± 2 mL/min/kg; P < 0.0001). HFpEF‐HT displayed a lower peak cardiac output (9.8 ± 0.9 L/min) compared to HT (12.6 ± 1.0 L/min; P = 0.02) and controls (13.3 ± 1.0 L/min; P = 0.01). Peak AVO2diff was reduced in HFpEF‐HT and HT (13.3 ± 2 and 13.5 ± 2 mL/dL vs. controls: 16.9 ± 2 mL/dL; P < 0.0001). A different left ventricular contractility was observed among groups, expressed as low‐load global longitudinal strain (−16.8 ± 5% in HFpEF‐HT, −18.2 ± 3% in HT, and 20.9 ± 3% in controls; P < 0.0001), and distribution of E/e′ and B‐lines [HFpEF‐HT: 13.7 ± 3 and 16, interquartile range (IQR) 10–22; HT: 9.5 ± 2 and 8, IQR 4–10; controls: 6.2 ± 2 and 0, IQR 0–2; P < 0.0001]. Conclusions Reduced peak VO2 values in HT with and without HFpEF may be the result of decreased AVO2diff. CPET‐ESE can also identify mild signs of left ventricular systo‐diastolic dysfunction and pulmonary congestion, promoting advances in personalized therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Cardiovascular and Pulmonary Function During Exercisementioning

confidence: 99%

Haemodynamic and metabolic phenotyping of hypertensive patients with and without heart failure by combining cardiopulmonary and echocardiographic stress test

Pugliese

Mazzola

Fabiani

et al. 2020

European J of Heart Fail

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“…Right ventricular (RV) dysfunction is frequently found in HFpEF as well, although the reported prevalence of RV dysfunction varies widely from 4% to 48% in individual studies . Although RV dysfunction in HFpEF has mainly been linked to the development of pulmonary hypertension (PH), RV remodelling in HFpEF may also occur in other conditions, independent of pulmonary pressures, such as shared risk factors for combined RV and LV dysfunction . It has been demonstrated that RV dysfunction is associated with poor prognosis, yet other studies were not able to observe such an association .…”

Section: Introductionmentioning

confidence: 99%

Right ventricular dysfunction in heart failure with preserved ejection fraction: a systematic review and meta‐analysis

Gorter

Hoendermis

Veldhuisen

et al. 2016

European J of Heart Fail

220

197

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“…However, in some patients with left-sided HF, superimposed pulmonary vascular remodeling occurs, and has been extensively reviewed elsewhere [57, 56, 58]. The cause of elevated pulmonary vascular resistance and/or diastolic pulmonary gradient (elevated PA diastolic pressure – pulmonary capillary wedge pressure gradient) in left-sided HF is likely multifactorial.…”

Section: Cardiorenal Syndrome Phosphate Balance and Pulmonary Hypermentioning

confidence: 99%

Visceral Congestion in Heart Failure: Right Ventricular Dysfunction, Splanchnic Hemodynamics, and the Intestinal Microenvironment

Polsinelli

Sinha

Shah

2017

Curr Heart Fail Rep

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Purpose of review Visceral venous congestion of the gut may play a key role in the pathogenesis of right-sided heart failure (HF) and cardiorenal syndromes. Here we review the role of right ventricular (RV) dysfunction, visceral congestion, splanchnic hemodynamics, and the intestinal microenvironment in the setting of right-sided HF. We review recent literature on this topic, outline possible mechanisms of disease pathogenesis, and discuss potential therapeutics. Recent Findings There are several mechanisms linking RV-gut interactions via visceral venous congestion which could result in (1) hypoxia and acidosis in enterocytes, which may lead to enhanced sodium-hydrogen exchanger 3 (NHE3) expression with increased sodium and fluid retention; (2) decreased luminal pH in the intestines which could lead to alteration of the gut microbiome which could increase gut permeability and inflammation; (3) alteration of renal hemodynamics with triggering of the cardiorenal syndrome; and (4) altered phosphate metabolism resulting in increased pulmonary artery stiffening, thereby increasing RV afterload. A wide variety of therapeutic interventions that act on the RV, pulmonary vasculature, intestinal microenvironment, and the kidney could alter these pathways and should be tested in patients with right-sided HF. Summary The RV-gut axis is an important aspect of HF pathogenesis that deserves more attention. Modulation of the pathways interconnecting the right heart, visceral congestion, and the intestinal microenvironment could be a novel avenue of intervention for right-sided HF.

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Pulmonary Hypertension Secondary to Heart Failure With Preserved Ejection Fraction

Cited by 33 publications

References 68 publications

Haemodynamic and metabolic phenotyping of hypertensive patients with and without heart failure by combining cardiopulmonary and echocardiographic stress test

Haemodynamic and metabolic phenotyping of hypertensive patients with and without heart failure by combining cardiopulmonary and echocardiographic stress test

Right ventricular dysfunction in heart failure with preserved ejection fraction: a systematic review and meta‐analysis

Visceral Congestion in Heart Failure: Right Ventricular Dysfunction, Splanchnic Hemodynamics, and the Intestinal Microenvironment

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